Loss of Bcl-G, a Bcl-2 family member, augments the development of inflammation-associated colorectal cancer

Paul M. Nguyen, Laura F. Dagley, Adele Preaudet, Nga Lam, Maybelline Giam, Ka Yee Fung, Kaheina Aizel, Gemma van Duijneveldt, Chin Wee Tan, Yumiko Hirokawa, Hon Yan K. Yip, Christopher G. Love, Ashleigh R. Poh, Akshay D’ Cruz, Charlotte Burstroem, Rebecca Feltham, Suad M. Abdirahman, Kristy Meiselbach, Ronnie Ren Jie Low, Michelle PalmieriMatthias Ernst, Andrew I. Webb, Tony Burgess, Oliver M. Sieber, Philippe Bouillet, Tracy L. Putoczki

Research output: Contribution to journalArticleResearchpeer-review

4 Citations (Scopus)


Gastrointestinal epithelial cells provide a selective barrier that segregates the host immune system from luminal microorganisms, thereby contributing directly to the regulation of homeostasis. We have shown that from early embryonic development Bcl-G, a Bcl-2 protein family member with unknown function, was highly expressed in gastrointestinal epithelial cells. While Bcl-G was dispensable for normal growth and development in mice, the loss of Bcl-G resulted in accelerated progression of colitis-associated cancer. A label-free quantitative proteomics approach revealed that Bcl-G may contribute to the stability of a mucin network, which when disrupted, is linked to colon tumorigenesis. Consistent with this, we observed a significant reduction in Bcl-G expression in human colorectal tumors. Our study identifies an unappreciated role for Bcl-G in colon cancer.

Original languageEnglish
Pages (from-to)742-757
Number of pages16
JournalCell Death and Differentiation
Issue number2
Publication statusPublished - Feb 2020


  • cancer models
  • tumour-suppressor proteins

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